ASPIRIN RESISTANCE AS A RISK MARKER FOR VENOUS THROMBOEMBOLIC COMPLICATIONS
M.V. Kruchinina1,2, A.A. Gromov1, A.V. Rabko1, P.A. Abdullaeva1, V.A. Baum1, V.M. Generalov3, K.V. Generalov3, V.N. Kruchinin4, S.V. Rykhlitskiy4, G.V. Shuvalov5
1Institute of Internal and Preventive Medicine - Branch of Federal Research Institute of Cytology and Genetics of SB RAS, 630089, Novosibirsk, Boris Bogatkov str., 175/1
2Novosibirsk State Medical University of Minzdrav of Russia, 630091, Novosibirsk, Krasny av., 52
3Federal Budgetary Research Institution В«State Research Center of Virology and Biotechnology В«Vector», Federal Service for Surveillance on Consumer Rights Protection and Human Well-being, 630559, Novosibirsk region, Koltsovo
4Rzhanov Institute of Semiconductor Physics of SB RAS, 630090, Novosibirsk, Academician Lavrentev av., 13
5Siberian State Order of the Red Banner of Labor Institute of Metrology, 630004, Novosibirsk, Dimitrov av., 4
Keywords: аспиринорезистентность, механизмы, маркер, риск, венозные тромбоэмболические осложнения, aspirin resistance, mechanisms, marker, risk, venous thromboembolic complications
Abstract
The possible mechanisms for the development of aspirin resistance, platelet involvement in thrombus formation, inflammation and atherogenesisare presented. The presence of associations between aspirin resistance and the risk of thrombotic complications in people not using aspirin and the possibility of using aspirin resistance to assess the individual risk of thromboembolic complications in 492 patients (mean age 56.2 ± 0.9 years) with arterial hypertension I - Stage II and without ithas been researched. The parameters of platelet aggregation were studied in subgroups of patients different in the risk of developing venous thrombo-embolic complications by reaction to the cyclooxygenase blocker. It has been revealed that the conducted antiplatelet therapy is effective in 50-60 % of persons with cardiovascular diseases; ~ 40 % of patients show signs of relative resistance to antiplatelet agents. Resistance to therapeutic doses of antiplatelet agents is multifactorial, however, the presence of a shunt between thromboxane synthetase and lipoxygenase plays a role in it. It is likely that the influence of inflammation on the development of aspirin resistance through an increase in the synthesis of 12-NETU, thromboxane and leukotrienes. Aspirin resistance is a risk factor for the development of venous thrombotic complications, regardless of the use of antiaggregant therapy. It was established that the most accurate prediction of the result according to the severity of hemorheological disorders (distinguishing between moderate and severe disorders from the lungs) is provided by such indicators of platelet aggregation as the coefficient K ((ADF5 % - ADP 5 % + Asp) - 100 / ADF 5 %) (AUC 0.995) and ADP 5 % (AUC 0.713). Changes in platelet aggregation in response to aspirin in an in vitro test can be used to identify individuals with a high risk of thrombotic complications, and to assess individual risk (specificity 92.9-98.2 %, sensitivity 83.7-93 %).
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